Archive for August, 2009

After a few weeks of debilitating illness in June and July I wasn’t sure whether or not to stick to my plan of running the Robin Hood half-marathon in September. When I started running again in late July I began with easy or moderate paced runs of around 5-6Km, it became clear that I had lost a lot of fitness, but I was enjoying running. Then at the beginning of August I decided to put matters to the test and ran 15Km, starting slowly but increasing the pace gradually. I was pleased to find that I felt comfortable at a pace around 5 min/Km in the second half of the run. That settled the question. I would run the half-marathon. I was uncertain about the target time to set myself, but provisionally set a target time of 100 min – only one minute slower than the target I had set several months earlier.

As for training strategy, my first objective was to try to re-establish a reasonable level of endurance; so I planned to build up the distance with fairly easy paced running, up to around 60 Km per week. By mid-August, things were going according to plan. I had three runs of 16-20Km behind me, and several ‘tempo’ runs – though at that stage, tempo pace was not much faster than 5 min/km. I planned do two easy-paced longish runs in the third week of August followed by a few upper aerobic runs to confirm my choice of target race pace. Then something peculiar happened.

Malign alien force or guardian angel?

On the third Monday of the month, I set out on the first of the two planned easy-paced longish runs. For about 5Km, things went well. I felt very relaxed running at a pace of 5:45 min/Km with a heart rate in the lower aerobic zone (around 122). And then quite unexpectedly, all the energy drained away from me. I struggled to maintain a pace of 6:30 min per Km. My heart rate dropped to around 115 and my legs felt very heavy. It appeared that I was battling some alien force. For the next few Km I made efforts to push the pace but then realized that it was a pointless struggle. It was clear that I was losing the battle against the alien influence. However, apart from the lethargy and heavy legs I was not experiencing any physical symptoms. My pulse was regular and strong, though reluctant to increase much above 115 bpm. So I kept on plodding along wondering what it all meant. In the end I covered 16 Km, but at times my pace dropped to 8 min/Km.

The next day I did a short easy jog and felt OK, so on the Wednesday I again attempted the planned long easy paced run, though on this occasion, aiming only for a pace around 6 min/Km. I felt sluggish though at least I was able to get my heart rate above 120. Again I managed to do16 Km, but it appeared that I was in no shape to race a half-marathon within a few weeks. I took it easy, doing only short easy runs for the rest of the week, and on the following Monday made yet another attempt at a longish run. Yet a third time, the alien force was holding me back. I eventually settled in for a slow plod at a pace in the range 6:30 to 6:45 min per Km and heart rate around 110.

What was going on? I had been experimenting with various fitness measures using my new Polar RS80CX heart rate monitor, and after some experimenting, I have decided that the orthostatic test appears to be the most practical and useful test for monitoring my response to training. What is clear is that during that third week of August I was experiencing an excessive parasympathetic drive that was keeping my heart rate down. Maybe I am not struggling against an alien force; more likely it is a tyrannical guardian angel that is trying to protect me from myself.

The orthostatic test

In the orthostatic test, heart rate is recorded lying down for three minutes and then standing for a similar period. Heart rate increases after standing, to elevate blood pressure sufficiently to combat pooling of blood in the lower extremities and thereby ensuring adequate perfusion of the brain. This increase in heart rate is achieved by a shift in the balance between the activity of sympathetic nervous system (the adrenaline-based fight or flight system) and the parasympathetic nervous system (which generally promotes relaxation and recovery). On standing, sympathetic activity increases and in a fit person, an increase in heart rate of around 10 bpm can be expected (McGee and Abernethy, Journal of the American Medical Association. 1999;281:1022–1029.). In an unfit or stressed person, the increase is usually greater.

However, sometimes there is a paradoxical surge of parasympathetic activity – blood pressure falls and the person collapses in a faint. Recovery usually follows quickly provided the person remains lying down. This paradoxical surge of parasympathetic activity – a so-called vasovagal attack- appears to reflect an over-active compensation mechanism that exists to prevent us from over exerting ourselves.

While a faint is transient and harmless, it is interesting to speculate on the similarities between a transient vasovagal event and two enigmatic conditions that are very relevant to athletes: fatigue and over-training. But first it is relevant to examine the results of a study of orthostatic test responses in marathon runners

Orthostatic responses after a marathon

Gratze and colleagues carried out an orthostatic test on 51 healthy amateur marathon runners the day before the Graz (Austria) marathon in 2007 and 2 hours after completion of the event (European Heart Journal vol 29, pp 1531–1541, 2008). None of the runners exhibited a vaso-vagal attack on the day before the race, but 14 did so on testing after the event. These runners were classified as orthostatic intolerant. As expected, all runners exhibited evidence of increased sympathetic activity (indicative of stress) after the event, but the 14 who were orthostatic intolerant were unable to generate the required increase in sympathetic activity to compensate for pooling of blood in the lower extremities during the test. Instead they demonstrated a paroxysmal increase in parasympathetic activity, and developed signs of incipient collapse.

The only significant predictor of risk of orthostatic intolerance identified by Gratze and colleagues was having serum potassium levels in the lower part of the normal range before the race. However there was also a trend towards a higher training volume in the preceding 4 weeks in the orthostatic intolerant group. (The probability that the difference between groups would have been as large as that observed purely by chance was 6.9%. Thus the possibility of chance cannot be ignored, but weighing up all the evidence makes me think that the difference is unlikely to be due to chance). The orthostatic intolerant group also had a higher training volume in their lightest week in the preceding month – in other words, they had not tapered to the same extent as those who did not develop orthostatic intolerance. This invites the speculation that the runners who developed orthostatic intolerance were on the verge of over-training.

Over-training

Improving fitness necessarily demands over-reaching – the transient deterioration in performance following hard training that stimulates the development of increased fitness during the subsequent recovery phase. If the athlete does not allow time for recovery following a hard training session, over-reaching develops into the early ‘sympathetic’ phase of the over-training syndrome, characterized by over-activity of the sympathetic nervous system – the adrenaline-related component of the autonomic nervous system that generates the fight or flight response. Provided this sympathetic phase of the over-training syndrome is recognized in time, reduction in training volume or intensity for a few days is usually enough to promote recovery.

However, if it is not recognized, non-conscious neural mechanisms intervene to protect us from our own fool-hardiness. Perhaps this guardian angel within our non-conscious mind might be described as the central governor – though this is not quite the context which led Tim Noakes to develop the central governor hypothesis. Whatever the true nature of our guardian, he/she is scarcely an angel and the consequences of his/her intervention are not quite what we might wish – the parasympathetic nervous system which normally promotes healthy relaxation and recovery becomes a tyrant.

The balance between parasympathetic and sympathetic activity tilts strongly towards parasympathetic excess. We no longer have any drive for fight or flight . We become listless, apathetic and find that getting the heart rate up into the upper aerobic zone demands a major effort. The body is unable to mount an adequate defence against either injury or illness, and eventually either injury or illness forces a cessation of training. This is the parasympathetic phase of the overtraining syndrome, and can last for weeks, months or even years. If the 14 individuals from the sample of 51 marathon runners studied by Gratze were indeed on the verge of the parasympathetic phase of the over-training syndrome, then the risk of this problem is not uncommon.

Wrestling with an over-protective nanny

One of the reasons I have become especially interested in the over-training syndrome in recent times is the fact that despite life-long mild asthma which had caused me no problems since infancy, I have been increasingly hampered by broncho-constriction, the defining characteristic of asthma, in the past two years. I have also been aware of having a rather low heart rate suggesting a tendency towards parasympathetic dominance. Broncho-constriction can be precipitated by parasympathetic over-activity. The sympathetic ‘fight or flight’ response opens the airways, while the parasympathetic ‘rest and recovery’ system has the opposite effect.

When I read Hadd’s well known account of his client Joe, who was training for a 2:20 marathon, I was intrigued to note for the first few levels of the Hadd test (a series of 2.4 Km runs at incrementally increasing heart rate) that I could run faster than Joe at a specified heart rate – though of course Joe could push his heart rate far higher than I could, and therefore he would have left me far behind in a race. Perhaps I was a more efficient runner than Joe at slow paces, but efficiency is less important than VO2 max for all events other than ultra-marathons.

I started to wonder whether or not the increased severity of my asthma and my low heart rate were evidence that some non-conscious part of my brain was taking action to prevent me over-exerting myself. On balance, this apparently hypothetical tyrannical guardian angel appears to be acting in my best interests, and in particular, is protecting my heart, but the tyranny felt as irksome as an over-protective nanny. It seemed worthwhile to get a heart rate monitor and try to wrestle some of the control back from this over-protective nanny.

Fatigue and the parasympathetic system

I hoped to use the monitor to maximse the efficiency of my training. However, I had not anticipated the effects of my recent illness – a protracted bout of chicken pox accompanied by various complications. In the aftermath of a viral illness there is risk of the enigmatic condition known variously as post-viral fatigue, myalgic encephalopathy (ME), or chronic fatigue. The name used depends on the individual’s personal investment in the problem. Many sufferers are adamant that it has a physical cause and tend to prefer terms like post-viral fatigue or ME; while skeptics tend to say it is all in the mind and prefer the term chronic fatigue.

I suspect that multiple causes contribute: there are predisposing factors, precipitating factors and maintaining factors. There is little doubt that viral illness can be a precipitating factor. Possibly a tendency towards low parasympathetic activity is a predisposing factor, although paradoxically, excessive anxiety and sympathetic activity might also be a precursor. There is a fairly large but inconsistent body of evidence indicating that the parasympathetic nervous system can be deranged in chronic fatigue – a confusing situation encapsulated in the title of a review article by Freeman ‘ The chronic fatigue syndrome is a disease of the autonomic nervous system: Sometimes.’ (Clinical Autonomic Research vol 12, pp. 231–233, 2002). Typically, cases of chronic fatigue show evidence of an incipient vaso-vagal attack during orthostatic testing.

Although the literature on chronic fatigue is largely to be found in journals of cardiovascular medicine, immunology or psychiatry, while the literature on over-training is confined to sports medicine journals, it is probable that the two conditions have much in common.

I also think there is little doubt that what I suffered in mid-August was the beginnings of a bout of post-viral fatigue. Although I had attempted to return to training fairly cautiously after my illness, my decision to persist with my plan to run a half-marathon probably led me to push myself a little too hard. I would not describe my present problem as an over-training syndrome yet, but I think I am on the edge.

Here is the record of my heart rate during the orthostatic test when my condition reached a nadir on 18th August, together with a more typical recording performed on 2nd August.

On 18th August, during the initial 3 minutes lying-down, my mean heart rate is 51 and there are high frequency fluctuations on a time scale of around 15 peaks /minute. During the 30 seconds following standing my pulse rises to 71 bpm but then, while remain standing, an excessive parasympathetic surge produces a fall to a mean value slightly lower than the value when lying down, at times falling below 40 bpm. It is noteworthy that the frequency of fluctuations decreases while standing relative to lying down, indicating greater sympathetic input, though the frequency while standing on 18th Aug is still higher than on 2nd August. The increase of 9 bpm from resting to standing on 2 August is typical

In contrast, the evidence from clinical trials indicates that carefully graded exercise can be beneficial (Larun and colleagues, Cochrane Database of Systematic Reviews 2004, Issue 3) The debate is heated because of the implication that if it can be cured by graded exercise, perhaps it was all in the mind after all. However, I think that view underestimates the amazing nature of the mind, and the brain that under-pins it.

The mind is no less real than the immune system or the cardiovascular system. Almost certainly non-conscious mechanisms in the mind (and its brain) act to protect us from ourselves. It is likely that the excess of parasympathetic activity that can occur in chronic fatigue is one such a mechanism. However, despite being clever, the non-conscious mind is not always wise, because it is dependent on the information we feed to it. If our conscious mind reinforces the need to be protective, it is possible to create a vicious circle in which conscious and non-conscious mechanisms get cemented into an over-defensive reaction. By judicious conscious efforts to test the limits, we might be able to train the non-conscious mind to adjust the tightness of the leash in an optimal manner.

If so, perhaps the most effective way of preventing incipient post-viral fatigue from becoming protracted debilitating chronic fatigue is to undertake carefully graded exercise so that the non-conscious mind/brain can adjust the tightness of the leash rather than consolidate the current status and create an intractable chronic problem.

Here is a graph showing the day-by-day variation in the difference between lying and standing heart rate during the orthostatic test.

After the nadir in mid-August, there was a fairly steady improvement. The red arrows mark days (both before and after the nadir) when I had increased training volume up to 15Km or more (albeit at a very easy pace). On each occasion, there was a deterioration on the following day. The blue arrows indicate days of complete rest. These are followed by improvement, but perhaps even more importantly, during the period including runs of gradually increasing intensity over short distances, from 25-29th August, the trend was strongly upwards. Over this period, the Poincare plot ( a two dimensional scatter-plot that illustrates variation in inter-beat intervals, and in particlar allows as estimate of the rapid beat-by-beat changes in interbeat interval produced by activity of the parasympathetic nervous system) revealed that increasing orthostatic rise in heart rate was accompanied by decreasing parasympathetic drive during the standing phase.

Many a slip between cup and lip.

On Saturday (29th August) I was sufficiently encouraged by my progress that I was tempted to increase training volume. I ran 15 Km, starting slowly and gradually increasing up to a pace around 5 min/Km, achieving an overall average pace of 5:24. This was a mistake. On Sunday morning, the orthostatic difference was back down to 1 bpm. This morning (Monday) it was 2 bpm. It was clear that I still need to take things cautiously.

I decided that instead of running today I would repeat a session on the elliptical cross-trainer which I had done in mid July, at a time when I was gradually building up the training-load after my illness. During the session, I increased the work-rate very gradually at 4 minute intervals, starting at 35 watts and increasing to 240 watts. When I had done this session in mid-July, I had exceeded the ventilatory threshold (where breathing become very deep and rapid) during the final two levels. My average heart rate in the final few minutes was 157 bpm (about 98% of maximum), but it had been an exhilarating rather than demanding session. I anticipated that despite my recent fatigue, the training I had done since early July would be enough to allow me to achieve a 240 watt output while barely exceeding the ventilatory threshold.

I felt reasonably relaxed during the early phases, though occasional glances at the heart rate monitor indicated that my pulse was rising at a similar rate to mid-July. And then at 200 watts, I hit a very solid wall. Suddenly I was gasping for breath. I could scarcely believe how difficult it was. However, it seemed that little harm could come from a few more minutes of exertion so I pushed on for the full 4 minutes of the 240 watt level. When I examined the heart rate recording I was stunned to see that my heart rate had stopped rising after reaching 143 bpm at the 200 watt level. The subsequent 240 watt level had felt so difficult because there had been no appreciable increase in cardiac output despite an increase in work-rate. In the final few minutes I must have been utilizing almost purely anaerobic metabolism. No wonder it felt difficult.

The Poincare plot confirmed that it was the parasympathetic system that had blocked further rise in cardiac output beyond the level reached at 200watts. A comparison of the Poincare plots in mid-July and today demonstrate that the variation along the 45 degree axis of the ellipse (largely due to sympathetic activity) was very similar on the two occasions: 6.9 ms in July compared with 5.6 ms today, but the variation across the 45 degree axis had increased more than threefold from 4.0 ms to 13.4 ms, indicative of a relatively large amount of parasympathetic activity. The consequence of this parasympathetic drive was a false ceiling on VO2max, and the sensation of hitting a solid wall. I wonder does this mechanism play a part in creating the wall dreaded by ill-prepared marathoners?

Poincare plots of R-R intervals over a 2 minute period during the 200 watt level in the elliptical session on 18th July and 31st August

The future

I must now steer a course between Scylla and Charybdis, the mythical monsters that guarded the Straits of Messina. If I push myself too hard the excessive stress will evoke an even more restrictive parasympathetic defense and I am likely to end up with protracted fatigue. However, the evidence from studies of chronic fatigue indicates that the dangers of molly-coddling myself are almost as great. Acute post viral fatigue can become very entrenched if the non-conscious mind/brain learns that the only safe path is low intensity activity.

Previously in such circumstances I would have been inclined to opt for slowly re-building of aerobic base with a Maffetone-style program. However, that would not be entirely logical as I think my aerobic base is still fairly robust. The observations of the past 10 days suggest that short, moderate intensity sessions might be more effective for promoting recovery, whereas longer runs are likely to lead to further deterioration.

As for my half-marathon plans, I will simply have to see what unfolds in the next 10 days. The Gratze study suggests that the two most crucial things to do in preparation are tapering, and ensuring that serum potassium level is not low. Unfortunately, one of the side effects of my asthma inhaler is a decrease in serum potassium, so there are other less fearsome but nonetheless potentially troublesome monsters circling not far below the surface as I attempt to cajole my over-protective nanny through the gap between Scylla and Charybdis. At this stage negotiating that gap is more important than the half-marathon, but provided my orthostatic test results show a moderate degree of normalization, I am inclined to at least present myself at the starting line.

I am now completely recovered from the illness that afflicted me seven weeks ago. The main symptoms had resolved after 4 weeks and I have gradually resumed training in the past few weeks, though prior to this morning, I my longest run had been 6.5Km, and the only session at a pace faster than 5:30 min per Km was a 4 Km tempo run.

This morning I faced the question of whether or not to abandon my plan to run a half marathon in early September. Seven weeks ago my training was progressing according to plan, and my target time of 99 minutes appeared reasonable. After four weeks of quite debilitating illness and 3 weeks of very light training, that target is probably beyond me. Is it even feasible to contemplate a half marathon at all, within the next 6 weeks?

Last night I had vacillated between planning a 10Km run as the first step in a prudent program directed at recovering endurance, or a moderately paced 15Km to force an answer to the question of whether or not I should persist with my plan for half marathon in early September. This morning, the rain was beating down from an oppressive leaden sky, and my initial inclination was towards a prudent 10K. However, rain often looks worse when seen though a glass window than it feels splashing on your face. So I decided on the 15K, starting slowly, but with the intention of increase pace gradually to around 5:15 min/Km.

The rain was invigorating and I gradually built up pace. During the second Km my heart rate monitor revealed some brief bursts of tachycardia (discussed below) but I felt fine so I continued to increase pace gradually, and still felt comfortable when I reached 5 min/Km. The rain continued to pour down and my clothes and shoes became water logged. I had set off in a pair of old, very heavy, reebok shoes because I suspected that the intrinsic muscles of my feet might have become de-conditioned in the past seven weeks, and I wanted to protect my awkwardly angled metatarsophalangeal joints from the stony sections of the riverside path. It was probably a wise decision, but nonetheless as I splashed through the mud and slush, the water-logged reeboks felt like soggy clogs. I had images of Emil Zatopek training in army boots and re-assured myself that I was probably giving my hamstrings and hip flexors a good work-out. From 3 Km to 15 Km I maintained a constant cadence of 186 strides per minute (except on the short steep hills) and I gradually increased my stride length from 104 cm to 110 cm. I finished comfortably with an average overall pace of 5:11 min per Km and a heart rate of 664 beats/Km.

So what conclusion should I draw? I felt relaxed and comfortable throughout. My only subsequent musculo-skeletal discomfort is some tenderness of the tissues overlying my metatarsophalangeal joints, confirming the anticipated de-conditioning of my feet during the past seven weeks. My larger muscles appear to have coped well. I could almost certainly run much faster in a half-marathon race. The heavy shoes and muddy surface probably cost me several minutes.

However, I am not sure that my former target of 99 minutes (4:42 min per Km) is within reach Today’s performance is very similar to my training runs in early June. At that stage, with three months preparation ahead of me, I was confident of achieving my target. Now, with only a month of training ahead, I doubt that 99 minutes is feasible, but am fairly confident that if all goes well during August, I can achieve a time of 102 min; maybe even 100 min. So I have set myself a provisional target of 100 min.

The Polar RS800CX

My new Polar RS800CX Heart Rate Monitor has provided me with lots of fascinating information, but at this stage, I am not sure what to make of it all.

Quality of the engineering

My first impression is that it is not as well engineered as I had anticipated for a Polar product. Sometimes the facilities if offers do not appear to work reliably; for example the first time I attempted to use the Own Optimizer test of training stress and recovery, it failed to give the beep after three minutes to signal that it was time to stand up. At other times it gives warnings of problems that do not appear to exist. At this stage I am monitoring the situation to determine whether any of these problems is sufficiently troublesome to justify returning the device to Polar. On account of the large number of clever options it provides, I suspect that have yet to learn many of its subtleties.

I am not sure about the S3 foot pod. It definitely gives unreliable estimates of distance if not mounted very firmly. I am not yet convinced that it is reliable even when firmly mounted. Sometimes it fails to communicate with the wrist-mounted watch/computer for a period of 10-15 seconds, and I am trying to ascertain if this is caused by running near large metal objects. However, despite occasional evidence of minor unreliability, my interim conclusion is that it is useful to have a reasonably reliable estimate of pace during training.

Heart rate variability

The more interesting thing is the information the RS800CX provides about my heart. There is no doubt the information is interesting, though whether this will allow me to train more effectively remains to be seen. I have been doing a recording each morning while seated and relaxed. This confirms that I produce a healthy amount of high frequency heart rate variability at approximately the respiratory frequency suggesting good function of the parasympathetic nervous system; the system that promotes relaxation and recovery. Figure 1 shows a typical 5 minute segment of resting heart rate. The fluctuations occur at approximately the breathing frequency (6 breaths per minute).

Figure 1: Five minutes of resting HR

I will be interested to see how the resting heart rate variability changes once I beginning training more heavily. As I anticipated, I am frustrated by the Polar Own Optimizer, which merely gives a single number indicating recovery status. It maybe that for a person who is not interested in the physiology, a single number is all that they want, but I suspect that reducing the relatively complex information contained within the heart rate recording to a single number creates the risk of erroneous interpretation in some circumstances.

So far, I am finding a strong correlation between the various indices of parasympathetic function derived from HRV and low resting heart rate. Maybe a simple observation of resting heart rate would be less prone to misinterpretation, though it should be noted that in the more severe form of the over-training syndrome, resting heart rate is likely to be mis-leadingly low due to over-compensation by the parasympathetic nervous system. So even a simple measurement such as resting HR needs to be interpreted in light of the overall evidence

Erratic HRV

The most interesting thing I have discovered about my own heart is that despite a healthy amount of heart rate variation associated with parasympathetic activity, my heart rate also exhibits some more erratic variability. Sometimes during warm-up I get brief runs of rather dramatic tachycardia, during which my heart beats much faster than the anticipated maximum rate of the normal pacemaker in the sinus node. With my old primitive HRM, I occasionally observed these events, but attributed them to malfunction of the monitor. However, with the detailed record of R-R intervals provided by the RS800CX I can examine these events in much greater detail, and they do appear to arise from aberrant initiation of the heart beat. However I cannot be certain of their origin until I record a full ECG. Figure 2 presents a comparison of a selected (atypically bad) one minute segment of the HR record during warm-up, with a typical one minute segment recorded in the mid-aerobic range. During the atypical warm-up segment, there is no evidence of fluctuation at the breathing rate, but instead there are erratic fluctuations including bursts of a few beats at a heart rate over 200 per minute, which is far above the maximum rate of my normal sinus node pace-setter (around 160 bpm). In the mid-aerobic segment the fluctuations are fairly regular at approximately the breathing rate (around 45 breaths per minute).

Figure 2: One minute segments of HR during warm-up and in mid aerobic zone

I am re-assured by the fact that there is growing evidence that ventricular tachycardia (which is potentially a precursor of fatal ventricular fibrillation) tends to be a predictor of cardiac death when it is observed during recovery rather than during exercise itself. In my case, the abnormalities are mainly present during warm-up. When I am working fairly hard, my heart rate exhibits an apparently healthy pattern of variation. As expected, the parasympathetic influence decreases markedly as I approach maximum heart rate, but there is still an appreciable variation at the respiratory frequency. Furthermore, during the recovery period, the parasympathetic influence re-asserts itself rapidly. So overall, I think I have a quite healthy heart (for a 63 year old) but it may be that there is an irritable bit of muscle in the walls of my ventricles that gets impatient with my well-regulated sinus node during warm-up. I will experiment with a more gradual warm-up.

In conclusion, perhaps my previous ignorance was bliss, but I am inclined to think that it is better to understand the situation more fully. Any middle aged person who runs vigorously faces a small risk of a heart attack. I suspect that in most cases, the increase in life expectancy due to the improved cardiac function produced by training far outweighs the small risk of catastrophe. I hope that the additional information provided by my HRM will allow me to improve the odds in favour of increased life expectancy.

However, for the person who would rather avoid the intricacies of interpretation, maybe the most sensible thing is simply to measure resting heart rate each morning. For the gung-ho individual, maybe even this seems over-academic – always looking both ways before crossing the road might provide a greater improvement in life-expectancy in proportion to effort spent. However I am enjoying the exploration of the intricacies of heart rate variability, and I am increasingly confident that it will allow me to regulate my training more effectively.